The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation

Citation
M. Kato et al., The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation, J HYPERTENS, 17(10), 1999, pp. 1395-1401
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
02636352 → ACNP
Volume
17
Issue
10
Year of publication
1999
Pages
1395 - 1401
Database
ISI
SICI code
0263-6352(199910)17:10<1395:TEOSPS>2.0.ZU;2-9
Abstract
Objective There is limited information on the mechanisms mediating the dele terious effects of passive smoke exposure. Cross-sectional studies indicate that nonsmokers exposed chronically to passive smoke have impaired endothe lium mediated vasodilation, We tested the hypothesis that acute exposure to sidestream (passive) smoke impairs endothelium-dependent vasodilation in h ealthy nonsmokers. Methods and results We studied 12 healthy nonsmokers (aged 27 +/- 5 years, nine men and three women). We obtained measurements of blood pressure, hear t rate, and bilateral forearm blood flow (FBF). Each individual was studied twice, following a randomized, placebo-controlled design. The effects of p assive smoke were studied on one day and the effects of vehicle (room air) on a separate day. Acetylcholine (ACh) and sodium nitroprusside (SNP) were infused into the left brachial artery before and after 15 min of exposure t o either passive smoke (carbon monoxide concentration between 20 and 40 p,p .m,) or vehicle (room air). The order of ACh and SNP, and smoke or vehicle, was randomized between individuals. Smoke exposure increased carboxyhemogl obin from 0.5 +/- 0.1% to 0.8 +/- 0.1% (P = 0.002). Neither passive smoke n or vehicle changed baseline measurements of heart rate, blood pressure and forearm vascular resistance (FVR), The vasodilatory responses to ACh and SN P were very similar, both before and after exposure to passive smoke and be fore and after vehicle. Conclusion Our data demonstrate that acute exposure to passive smoke does n ot alter either endothelium-dependent or independent vasodilatory responses in healthy nonsmoking individuals. Hence, impaired endothelial vasodilator y responses in nonsmokers chronically exposed to passive smoke most likely reflect chronic functional and/or structural changes in responses to cigare tte smoke, rather than the acute effects of cigarette smoke toxicity on end othelial function. J Hyperfens 1999, 17:1395-1401 (C) Lippincott Williams & Wilkins.